Cited by 119Air Quality and Health ImpactsIndoor Air Quality and Microbial ExposureMitochondrial Function and Pathology

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

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Guo, Zhiqiang, Hong, Zhicong, Dong, Weiyang, Deng, Congrui, Zhao, Renwu, Xu, Jian, Zhuang, Guoshun, Zhang, Ruxin·2017·International Journal of Environmental Research and Public Health

Abstract

Exposure to PM2.5 (particulate matter ≤2.5 μm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na+K+-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na+K+-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.

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Authors
Guo, Z., Hong, Z., Dong, W., Deng, C., Zhao, R., Xu, J., Zhuang, G., & Zhang, R.
Affiliations
Fudan University (CN)
Corresponding author
Zhang, Ruxin
Venue
International Journal of Environmental Research and Public Health
Publisher
MDPI AG
Published
2017-01-29
Volume
14
Issue
2
Pages
134
ISSN
1660-4601 (ISSN-L)
OpenAlex
W2582797467
Cited by
119
References
22
Citations by year
2026: 9 · 2025: 16 · 2024: 11 · 2023: 15 · 2022: 15 · 2021: 17 · 2020: 15 · 2019: 9 · 2018: 7 · 2017: 5
FWCI
5.31
Type
journal article
Language
en
Open access
Locations
  • International Journal of Environmental Research and Public Health (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
The National Natural Science Foundation of China (Grant No. 81371078)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
PM2.5, particulate matter, nasal mucosa, oxidative stress, mitochondrial damage, mitochondrial fission and fusion, mitochondrial dysfunction, air pollution toxicity, inflammation, Na+/K+-ATPase, Ca2+-ATPase, superoxide dismutase, malondialdehyde, OPA1, Mfn1, Fis1, Drp1, nasal lesions
MeSH terms
Air Pollutants, Animals, Disease Models, Animal, Female, Inflammation, Malondialdehyde, Mitochondria, Nasal Mucosa, Particle Size, Tumor Necrosis Factor-alpha, Interleukin-6, Interleukin-8, Oxidative Stress, Mitochondrial Proteins, Rats, Particulate Matter

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